Various molecular mechanisms are associated with the pathogenesis and progression of ALI, including inflammatory responses, oxidative stress, vascular endothelial cell proliferation, migration, apoptotic, immune system process, etc. Meanwhile, ALI and ARDS also have the characteristic of excessive neutrophil and macrophage infiltration into the lung tissues, release of pro-inflammatory cytokines (such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α) and lung endothelial and epithelial injuries as well, resulting in edema and gas exchange deterioration [5,6,7,8]. Here, TNF is linked to acute respiratory distress syndrome.